Abstract
Background: Low vital capacity, one of the consequences of restricted lung growth, is a strong predictor of cardiovascular mortality. Vital capacity is lower in the developing world than the developed world, even after adjusting for height, weight and gender. This difference is typically dismissed as ethnic variation, adjusted for by redefining normal. Whether this is a consequence of stunted lung growth, rather than just genetically smaller lungs, has not been investigated in detail. Therefore, we sought to compare factors implicated in both stunting and lung development, particularly in the developing world. Methods: We conducted a manual screen of articles identified through Google Scholar and assessed risk of bias. No language restrictions were applied, so long as there was an associated English abstract. We queried VizHub (Global Burden of Disease Visualization Tool) and Google Dataset search engines for disease burden and genome wide association studies. The scope of the article and the heterogeneity of the outcome measures reported required a narrative review of available evidence. To the extent possible, the review follows PRISMA reporting guidelines. Results: Early life influences operate in synergism with genetic, environmental and nutritional factors to influence lung growth and development in children. Low lung function and stunting have common anthropometric, environmental and nutritional correlates originating during early development. Similar anthropometric correlates shared chronic inflammatory pathways, indicated that the two conditions were analogous. Conclusion: The analogy between poor lung function and stunting is conspicuous in the developing world, with malnutrition at the center of non -achievement of growth potential, susceptibility to infectious diseases and intrauterine programming for metabolic syndrome. This counter the idea of redefining the normal for lung function measurements, since observed inter-ethnic variations are likely a mix of natural genetic differences as well as differences in nurture such that reduced lung function reflects early life adversities.
Highlights
Forced Vital Capacity normalized to height was found to be an independent indicator of cardiovascular risk in the Framingham Heart Study Cohort
We identified relevant articles using the search terms grouped according to risk factors, such as maternal nutrition and anthropometry, nutrition, anthropometry, environmental factors, sanitation, genetic and epigenetic factors
Higher burden of stunting and low lung function in the developing world indicates the role of socioeconomic influences Evidence of reduced lung function in the developing world emerged from the Prospective Rural Urban Epidemiological Study (PURE), which investigated global variation in lung function in healthy populations by region
Summary
A series of landmark studies since have cemented the role of spirometry as a prognostic tool for non-communicable disease outcomes in general and cardiovascular disease outcomes in particular[1,2,3,4,5,6] This has allowed lung function to transcend its status as an indicator of respiratory disease severity to a predictor of all-cause and cause specific mortality. Conclusion: The analogy between poor lung function and stunting is conspicuous in the developing world, with malnutrition at the center of non -achievement of growth potential, susceptibility to infectious diseases and intrauterine programming for metabolic syndrome.
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